CCM1/2 proteins control β1 integrin–dependent distribution of traction forces and FN remodeling. (A) pMLC and zyxin delocalized from the peripheral focal adhesions to transversal actin stress fibers upon depletion in ICAP-1, CCM1, or CCM2 after 4 h of spreading. Bar, 5 µm. These images are presented again in Fig. S3 C, where it is shown that pMLC and zyxin relocalized to the cell periphery upon additional silencing of β1 integrin but not of β3 integrin. (B) Representative traction forces maps obtained by TFM. Forces were delocalized from the cell periphery to all over the ventral face upon CCM depletion. (C) Quantification of the percentage of cells displaying central traction forces. Between 14 and 23 cells of each were analyzed. Error bars are means ± SEM (n = 2). Similar fold-increase of the percentage of cells bearing central forces was measured for CCM1-depleted HUVECs (n = 1; not depicted). Bar, 10 µm. Remodeling of glass-coated FN was studied on sparse cells after 24 h (D) and on confluent cells after 48 h (E). Bars, 5 µm. FN staining in the yellow box in E is magnified to highlight the linear pattern of parallel FN fibers produced by ICAP-1/CCM-depleted HUVECs. Bars, 2 µm. These data are representative of more than three independent experiments.